Background—
This study sought to test whether intracardiac echocardiography (ICE) is superior to conventional monitoring in guiding device closure of interatrial communications (atrial septal defect [ASD] and patent foramen ovale [PFO]).
Methods and Results—
Forty-four patients undergoing device closure of ASD (n=6) or PFO (n=38) were randomized to have the procedure guided by either ICE (group 1; n=22) or by transesophageal echocardiography (TEE) (group 2; n=22). All interventions were completed successfully. In 1 patient from group 2, atrial fibrillation occurred 1 day after device implantation; the patient was successfully cardioverted on the next day. There were no other complications. Fluoroscopy time (FT) (6.0±1.7 minutes versus 9.5±1.6 minutes;
P
<0.0001) as well as procedure time (PT) (33.4±4.7 minutes versus 37.8±5.6 minutes;
P
<0.01) were shorter in group 1 than in group 2. Group 2 patients required general anesthesia without (n=19) or with endotracheal intubation (n=3). In contrast, ICE allowed continuous monitoring of the whole procedure, including balloon sizing before device closure, without sedation.
Conclusions—
ICE is a safe tool to guide device closure of PFO and ASD. Supine patients tolerate ICE better than TEE. ICE reduces FT and PT. ICE seems to be advantageous, especially when long continuous or repeated echocardiographic viewing is required.
Basaloid squamous cell carcinoma (BSCC) of the esophagus is a rare, poorly differentiated variant of typical esophageal squamous cell carcinoma (SCC) characterized by high proliferative activity and frequent spontaneous apoptoses. In the present study, we investigated the expression of the apoptosis-suppressing protein Bcl-2 in 23 BSCC of the esophagus and 23 stage-matched typical esophageal SCC by means of immunohistochemistry. In addition, amplification of the apoptosis- and proliferation-inducing gene c-myc was determined by means of differential polymerase chain reaction. Bcl-2 expression was found significantly more often in BSCC than in SCC (86.9% vs. 17.4%, P < 0.0001). Amplification of c-myc was nearly twice as common in BSCC as in SCC (47.8% vs. 26.1%, not significant). Bcl-2 protein expression together with c-myc amplification was detected in 43.5% of the BSCC but in none of the typical SCC (P < 0.0001). Taken together, our findings indicate that the molecular pathogenesis of esophageal BSCC differs from that of typical SCC and frequently involves coactivation of c-myc and Bcl-2.
Barrett esophagus (BE) is a condition in which the normal squamous epithelium of the esophagus is replaced by a metaplastic columnar epithelium. BE is a premalignant lesion that represents the initial step in a metaplasia-dysplasia-carcinoma sequence. In the present study, amplification of the proto-oncogene c-myc was determined by means of differential polymerase chain reaction analysis of metaplastic specialized epithelium, low-grade dysplasia, high-grade dysplasia, and invasive adenocarcinoma obtained by microscopic dissection of 43 esophagectomy specimens. Amplification of c-myc was found in none of 29 specialized epithelial specimens, none of 23 low-grade dysplasia specimens, 6 of 24 high-grade dysplasia specimens, and 17 of 39 adenocarcinoma specimens. Our data indicate that amplification of c-myc is a late event in the metaplasia-dysplasia-carcinoma sequence in BE. Furthermore, determination of c-myc amplification may help identify high-risk patients who would benefit from intensified endoscopic surveillance or from immediate treatment.
In this all-comers registry, the use of the Pulsar-18 self-expanding nitinol stent in femoropopliteal lesions averaging 111.5 mm long showed promising primary patency and freedom from TLR after 6 and 12 months. Diabetes had no negative impact on patency. Primary patency in the popliteal segments was acceptable at 12 months.
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